A 47-year-old woman comes to the office for follow up of an asthma exacerbation. The patient was recently hospitalized and required a prolonged period of mechanical ventilation as well as nebulized bronchodilators and intravenous glucocorticoids. Her symptoms improved, and she was discharged on oral prednisone. The patient reports compliance with therapy. She has no other medical conditions and takes no other medications. Blood pressure is 128/72 mm Hg, pulse is 85/min, and respirations are 18/min. On physical examination, there is mild expiratory wheezing. Because of the persistent respiratory findings, the patient is continued on the same treatment regimen. Long-term administration of this oral therapy is most likely to increase which of the following in this patient?

Question

A 47-year-old woman comes to the office for follow up of an asthma exacerbation.  The patient was recently hospitalized and required a prolonged period of mechanical ventilation as well as nebulized bronchodilators and intravenous glucocorticoids.  Her symptoms improved, and she was discharged on oral prednisone.  The patient reports compliance with therapy.  She has no other medical conditions and takes no other medications.  Blood pressure is 128/72 mm Hg, pulse is 85/min, and respirations are 18/min.  On physical examination, there is mild expiratory wheezing.  Because of the persistent respiratory findings, the patient is continued on the same treatment regimen.  Long-term administration of this oral therapy is most likely to increase which of the following in this patient?

Quizplus · Accepted Answer

11ec160b_3bab_5c9f_9249_f105991da2b0_MD0001_00 Glucocorticoids are potent stimulators of liver gluconeogenesis and upregulate the synthesis of key gluconeogenic enzymes (eg, phosphoenolpyruvate carboxykinase, glucose-6-phosphatase). Glucocorticoids also increase hepatic glycogen reserves by increasing expression of glycogen synthase, thereby improving glucose availability during periods of acute stress. The increased demand for metabolic enzymes required for these actions leads to an overall increase in liver protein synthesis. Peripherally, glucocorticoids antagonize the actions of insulin in skeletal muscle, favoring catabolism and proteolysis to provide substrates for gluconeogenesis and glycogenesis in the liver (Choice E). This effect can manifest as proximal muscle weakness (glucocorticoid myopathy). The effect on adipose tissue is mixed, with lipolytic and antilipolytic effects, altered fat distribution (eg, central obesity, hypertrophy of the dorsocervical fat pad), and increased appetite and caloric intake. The net effect of gluconeogenesis and insulin antagonism is hyperglycemia. (Choice A) Long-term glucocorticoid therapy causes atrophy of the adrenal cortex. On abrupt cessation, the delay in resumption of endogenous cortisol production can precipitate acute adrenal insufficiency. (Choice B) Glucocorticoids inhibit fibroblast proliferation and collagen formation in the skin. This results in thinning of the skin, impaired wound healing, and stria. The connective tissue that supports the capillaries is also thinned, leading to easy bruising. (Choice D) Glucocorticoids are potent immunosuppressive agents. They increase expression of anti-inflammatory proteins but decrease expression of inflammatory proteins and cytokines and induce apoptosis in T cells (transient lymphopenia is common). Circulating neutrophil counts may increase in acute glucocorticoid administration due to increased release from bone marrow and "demargination" from peripheral tissues. (Choice F) Glucocorticoids decrease bone mass by multiple mechanisms, including decreased gastrointestinal calcium absorption, increased renal calcium excretion, and direct inhibition of osteoblast activity. Educational objective: Glucocorticoids are predominantly catabolic, causing muscle weakness, skin thinning, impaired wound healing, osteoporosis, and immunosuppression. However, they also cause increased hepatic synthesis of gluconeogenic and glycogenic proteins to increase glucose availability. This, along with peripheral antagonism of insulin, contributes to the development of hyperglycemia. __________ References: The effects of glucocorticoids on adipose tissue lipid metabolism. (http://www.ncbi.nlm.nih.gov/pubmed/21864867)

A 47-Year-Old Woman Comes to the Office for Follow Up